Evidence map›Paper›PMID 23209420›Full record

ArticlePLoS pathogens2012

Unique biofilm signature, drug susceptibility and decreased virulence in Drosophila through the Pseudomonas aeruginosa two-component system PprAB.

Sophie de Bentzmann, Caroline Giraud, Christophe S Bernard, Virginie Calderon, Friederike Ewald, Patrick Plésiat, Cathy Nguyen, Didier Grunwald, Ina Attree, Katy Jeannot and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.0field-weighted citation impact, top 14% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

38 citing papers in PubMed, 70 citations in OpenAlex.

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  5. Review
  6. Insights into Kinases of ESKAPE Pathogens for Therapeutic Interventions.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Review
  7. Article
  8. Article
  9. Transcriptional Regulators Controlling Virulence inInternational journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Article
  13. Biofilms and Benign Colonic Diseases.International journal of molecular sciences · 2022
    Review
  14. Article
  15. Review
  16. Conquering the host:Frontiers in microbiology · 2022
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

12 authors at 8 institutions in 1 country.

Sophie de BentzmannLaboratoire d'Ingénierie des Systèmes Macromoléculaires, CNRS - Aix Marseille University, Marseille, France. bentzman@imm.cnrs.fr
Caroline Giraud
Christophe S Bernard
Virginie Calderon
Friederike Ewald
Patrick Plésiat
Cathy Nguyen
Didier Grunwald
Ina Attree
Katy Jeannot
Marie-Odile Fauvarque
Christophe Bordi
Centre National de la Recherche Scientifique · FRLaboratoire d'Ingénierie des Systèmes Macromoléculaires · FRUniversité de franche-comté · FRAix-Marseille Université · FRCEA Grenoble · FRTheories and Approaches of Genomic Complexity · FRUniversité Joseph Fourier · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial biofilm is considered as a particular lifestyle helping cells to survive hostile environments triggered by a variety of signals sensed and integrated through adequate regulatory pathways. Pseudomonas aeruginosa, a Gram-negative bacterium causing severe infections in humans, forms biofilms and is a fantastic example for fine-tuning of the transition between planktonic and community lifestyles through two-component systems (TCS). Here we decipher the regulon of the P. aeruginosa response regulator PprB of the TCS PprAB. We identified genes under the control of this TCS and once this pathway is activated, analyzed and dissected at the molecular level the PprB-dependent phenotypes in various models. The TCS PprAB triggers a hyper-biofilm phenotype with a unique adhesive signature made of BapA adhesin, a Type 1 secretion system (T1SS) substrate, CupE CU fimbriae, Flp Type IVb pili and eDNA without EPS involvement. This unique signature is associated with drug hyper-susceptibility, decreased virulence in acutely infected flies and cytotoxicity toward various cell types linked to decreased Type III secretion (T3SS). Moreover, once the PprB pathway is activated, decreased virulence in orally infected flies associated with enhanced biofilm formation and dissemination defect from the intestinal lumen toward the hemolymph compartment is reported. PprB may thus represent a key bacterial adaptation checkpoint of multicellular and aggregative behavior triggering the production of a unique matrix associated with peculiar antibiotic susceptibility and attenuated virulence, a particular interesting breach for therapeutic intervention to consider in view of possible eradication of P. aeruginosa biofilm-associated infections.

Indexed as

Adhesins, BacterialAnimalsBacterial Secretion SystemsBiofilmsCell LineDrosophila melanogasterFimbriae, BacterialPseudomonas aeruginosaAdhesins, BacterialBacterial Secretion Systems

Identifiers

PMID23209420
PMCPMC3510237
OpenAlexW2025737378

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.